Dietary Tryptophan downregulates the gene expression of lipopolysaccharide-induced genes in healthy pigs susceptible to Enterotoxigenic E. coli K88

An important mechanism in regulating immunological and neurological responses is the catabolism of tryptophan (Trp). The pool of enzymes that break down Trp through the kynurenine pathway (so called from one of the final products) are found in numerous cell types, including cells of the immune system. Some of these enzymes are induced by some inflammatory signals. Thus, tissue inflammatory condition can cause depletion of tryptophan. This raises the hypothesis that intestinal infections could increase the requirement of Trp. Supplementary L-Trp limited the decrease of feed intake and growth in Enterotoxigenic E. coli K88 (ETEC) susceptible pigs, upon oral challenge with this pathogen (Trevisi et al., 2009). Our aim was to assess if genes involved in the intestinal barrier are changed by dietary Trp in healthy pigs susceptible or not to ETEC. Tryptophan favourably interacted to reduce the induction of lipopolysaccharide on genes involved in the intestinal barrier in ETEC susceptible pigs, but the causative mechanism needs to be established.